首页> 外文期刊>Journal of anesthesia >Comparison of the effects of vasopressin and norepinephrine on organ perfusion during septic shock in streptozotocin-induced diabetic rats.
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Comparison of the effects of vasopressin and norepinephrine on organ perfusion during septic shock in streptozotocin-induced diabetic rats.

机译:加压素和去甲肾上腺素对链脲佐菌素诱发的糖尿病大鼠感染性休克期间器官灌注的影响的比较。

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PURPOSE: The purpose of this study was to compare the effects of norepinephrine (NE) and vasopressin on systemic hemodynamics, renal and mesenteric artery blood flow, inflammatory response and inducible nitric oxide synthase (iNOS) activity during endotoxin shock in streptozotocin-induced diabetic rats. METHODS: The study was designed to include three sets of experiments: (1) measurement of changes in systemic hemodynamics and mesenteric and renal artery blood flow; (2) measurement of biochemical variables; and (3) measurement of iNOS activity in the mesenteric artery. Systemic hemodynamics, regional artery blood flow changes and biochemical variables were assessed before treatment and 1, 2 and 3 h after treatment. RESULTS: Vasopressin, but not NE, prevented the decreases in aortic blood flow, but did not restore mesenteric artery blood flow. In addition, vasopressin partially restored renal artery blood flow in diabetic rats. Plasma nitrite levels and iNOS activity in the mesenteric artery were elevated after intravenous LPS in diabetic rats. Endotoxin-induced decreases in mesenteric arterial blood flow were partially restored by vasopressin with nonselective NOS inhibitor, N G-nitro-l-arginine methyl ester (l-NAME), in diabetic rats. Moreover, l-NAME prevented increases in plasma nitrite levels and iNOS activity in the mesenteric artery. In contrast, endotoxin-induced decreases in renal arterial blood flow were partially restored by vasopressin with l-NAME, but not by NE in diabetic rats. CONCLUSIONS: Nitric oxide may be one possible contributor to reduced sensitivity of the mesenteric and renal arteries to vasopressin during septic shock in streptozotocin-induced diabetic rats.
机译:目的:本研究的目的是比较去甲肾上腺素(NE)和加压素对链脲佐菌素诱发的糖尿病大鼠内毒素休克期间全身血流动力学,肾脏和肠系膜动脉血流量,炎症反应和诱导型一氧化氮合酶(iNOS)活性的影响。 。方法:该研究被设计为包括三组实验:(1)测量全身血流动力学以及肠系膜和肾动脉血流的变化; (2)生化变量的测量; (3)测量肠系膜动脉中的iNOS活性。在治疗前以及治疗后1、2和3小时评估全身血流动力学,局部动脉血流变化和生化变量。结果:加压素而不是NE阻止了主动脉血流量的减少,但并未恢复肠系膜动脉的血流量。此外,加压素可部分恢复糖尿病大鼠的肾动脉血流。糖尿病大鼠静脉注射LPS后,肠系膜动脉血浆亚硝酸盐水平和iNOS活性升高。内毒素诱导的肠系膜动脉血流量减少可通过加压素与非选择性NOS抑制剂N G-硝基-1-精氨酸甲酯(l-NAME)的结合在糖尿病大鼠中得以部分恢复。此外,l-NAME阻止了肠系膜动脉中血浆亚硝酸盐水平和iNOS活性的增加。相比之下,内毒素诱导的肾动脉血流量减少可通过带有l-NAME的加压素部分恢复,但不能被糖尿病大鼠的NE恢复。结论:一氧化氮可能是在链脲佐菌素诱发的糖尿病大鼠败血性休克期间肠系膜和肾动脉对血管加压素敏感性降低的可能原因之一。

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